This, in turn, triggers the rapid and dynamic activation of Ca2+/calmodulin-sensitive NO synthases (NOS), such as through Ser1177 phosphorylation and activation of eNOS, promoting the synthesis of NO from l-Arg.

We have recently reported the upregulation of kinin B1 and B2 receptors at the same pain model and time frame [34], both of which cause elevated free intracellular calcium upon activation [35] that may contribute to the activation of both NOS isoforms.

RESULTS: Exposure of TMJ fibrochondrocytes to rHuIL-1beta resulted in the induction of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2), which were paralleled by NO and PGE2 production.

An alternative explanation for the bilateral expression of NOS isoforms in monoarthritic rats could be that the process of disease spreads to the contralateral side, thereby stimulating the upregulation of certain molecules (namely NOS) in the contralateral dorsal horn.

RESULTS: Exposure of TMJ fibrochondrocytes to rHuIL-1beta resulted in the induction of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2), which were paralleled by NO and PGE2 production.

Sympathetic nerve activation during sepsisappears to depend on the induction of NOS and COX; the COX pathway is involved in the elevation of temperature and in the activation of sympathetic nerve activity but not in the hypotension.

The mitochondrial adaptive response of mtNOS in neurodegenerative diseases is speculated as an increased mtNOS activity that supports an increased mitochondrial biogenesis in order to provide an increased energy supply.